Behavioral improvement in dystrophic mdx23 mouse following repeated antisense oligonucleotides injections Article Swipe
A. Aghaeipour
,
Mitsogiannis
,
Claire Fergus
,
K. Tetorou
,
Gileadi TE
,
E Stojek
,
Susana Pérez Talavera
,
S Singh
,
M. Siddle
,
Prendeville JA
,
Ewa Sokołowska
,
Kelly VP
,
Morgan JE
,
Federica Montanaro
,
Francesco Muntoni
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1016/j.omtn.2025.102750
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1016/j.omtn.2025.102750
Duchenne muscular dystrophy (DMD) is a severe neuromuscular disorder caused by mutations in the DMD gene that disrupt the production of functional dystrophin proteins. Intellectual disability and neurobehavioral complications including autism spectrum disorder, attention-deficit disorders, and anxiety cumulatively occur in 33%–43% of the patients due to deficiency of multiple dystrophin isoforms produced in brain. Previous work also identified behavioral abnormalities in the mdx23 mouse model of DMD. In this work we mapped the expression of the different dystrophin isoforms in different areas of the mouse brain. Next, we determined the behavioral phenotypes that best differentiate mdx23 (lacking the Dp427 isoform) and wild-type mice. Finally, we investigated the response to intracisternal magna (ICM) injection of exon-skipping phosphorodiamidate morpholino oligomer (PMO) antisense oligonucleotides, which induces skipping of exon 23 and restores the reading frame on these phenotypes. PMO administration led to low, detectable, restoration of dystrophin protein and DMD exon skipping in different brain regions. Treated mdx23 male mice exhibited a small but significant rescue of their enhanced fear response. We conclude that ICM delivery of PMO leads to low levels of dystrophin restoration, but these levels are sufficient to elicit a modest behavioral phenotype in mdx23 mice.
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- Language
- en
- Landing Page
- https://doi.org/10.1016/j.omtn.2025.102750
- OA Status
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- References
- 85
- OpenAlex ID
- https://openalex.org/W4415534196
All OpenAlex metadata
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https://openalex.org/W4415534196Canonical identifier for this work in OpenAlex
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https://doi.org/10.1016/j.omtn.2025.102750Digital Object Identifier
- Title
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Behavioral improvement in dystrophic mdx23 mouse following repeated antisense oligonucleotides injectionsWork title
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articleOpenAlex work type
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enPrimary language
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2025Year of publication
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2025-10-25Full publication date if available
- Authors
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A. Aghaeipour, Mitsogiannis, Claire Fergus, K. Tetorou, Gileadi TE, E Stojek, Susana Pérez Talavera, S Singh, M. Siddle, Prendeville JA, Ewa Sokołowska, Kelly VP, Morgan JE, Federica Montanaro, Francesco MuntoniList of authors in order
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https://doi.org/10.1016/j.omtn.2025.102750Publisher landing page
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://doi.org/10.1016/j.omtn.2025.102750Direct OA link when available
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0Total citation count in OpenAlex
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85Number of works referenced by this work
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| abstract_inverted_index.different | 76, 80, 150 |
| abstract_inverted_index.disorder, | 32 |
| abstract_inverted_index.dystrophy | 2 |
| abstract_inverted_index.exhibited | 157 |
| abstract_inverted_index.including | 29 |
| abstract_inverted_index.injection | 112 |
| abstract_inverted_index.mutations | 11 |
| abstract_inverted_index.phenotype | 192 |
| abstract_inverted_index.proteins. | 23 |
| abstract_inverted_index.response. | 167 |
| abstract_inverted_index.wild-type | 101 |
| abstract_inverted_index.behavioral | 58, 90, 191 |
| abstract_inverted_index.deficiency | 46 |
| abstract_inverted_index.determined | 88 |
| abstract_inverted_index.disability | 25 |
| abstract_inverted_index.disorders, | 34 |
| abstract_inverted_index.dystrophin | 22, 49, 77, 143, 180 |
| abstract_inverted_index.expression | 73 |
| abstract_inverted_index.functional | 21 |
| abstract_inverted_index.identified | 57 |
| abstract_inverted_index.morpholino | 116 |
| abstract_inverted_index.phenotypes | 91 |
| abstract_inverted_index.production | 19 |
| abstract_inverted_index.sufficient | 186 |
| abstract_inverted_index.detectable, | 140 |
| abstract_inverted_index.phenotypes. | 134 |
| abstract_inverted_index.restoration | 141 |
| abstract_inverted_index.significant | 161 |
| abstract_inverted_index.Intellectual | 24 |
| abstract_inverted_index.cumulatively | 37 |
| abstract_inverted_index.investigated | 105 |
| abstract_inverted_index.restoration, | 181 |
| abstract_inverted_index.abnormalities | 59 |
| abstract_inverted_index.complications | 28 |
| abstract_inverted_index.differentiate | 94 |
| abstract_inverted_index.exon-skipping | 114 |
| abstract_inverted_index.neuromuscular | 7 |
| abstract_inverted_index.administration | 136 |
| abstract_inverted_index.intracisternal | 109 |
| abstract_inverted_index.neurobehavioral | 27 |
| abstract_inverted_index.attention-deficit | 33 |
| abstract_inverted_index.oligonucleotides, | 120 |
| abstract_inverted_index.phosphorodiamidate | 115 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 15 |
| citation_normalized_percentile.value | 0.54273298 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |